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Dendrobium Officinale Kimura et Migo Ameliorates Insulin Resistance in Rats with Diabetic Nephropathy

Ming Zhao, Jungang Han

Research and Development Department, Shanghai Sanxiang Investment holdings Co., Ltd., Shanghai, China (mainland)

Med Sci Monit Basic Res 2018; 24:84-92

DOI: 10.12659/MSMBR.909242

Available online:

Published: 2018-05-31


#909242

BACKGROUND: Emerging evidence suggests the potential of Dendrobium officinale Kimura et Migo (DO) in treating the complications of diabetes mellitus (DM). We evaluated the therapeutic potential of DO in treating diabetic nephropathy (DN) by preventing insulin resistance.
MATERIAL AND METHODS: A DN model was established. Mean glomerular volume of rats was estimated by the method of Weibel-Gomez. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression of mRNAs and we used Western blot assay to determine the expression of proteins. The levels of fasting insulin (FINS) and glucagon (GLU) were measured and we assessed the levels of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-a (TNF-a), and interleukin-6 (IL-6) using the enzyme-linked immunosorbent assay (ELISA).
RESULTS: Compared with the Normal rats, the levels of urinary glucose, albuminuria, Scr, albuminuria/Scr and BUN, and the expression levels of CaN, TLR-2, TLR-4, MyD88, hs-CRP, TNF-a, and IL-6, the level of FINS, GLU, and HOMAIR were increased in DN, DO 1.0, DO 2.0, and DMBG groups. Compared with the DN rats, in DO 1.0, DO 2.0, and DMBG groups the glomerular volume was smaller, the levels of urinary glucose, albuminuria, Scr, albuminuria/Scr, and BUN, the expression levels of CaN, TLR-2, TLR-4, MyD88, hs-CRP, TNF-a, and IL-6, the level of FINS, GLU, and HOMA-IR were decreased.
CONCLUSIONS: We found that DO prevents insulin resistance in rats with DN. This may be associated with reduction of TLRs and inflammatory response, which should be further verified by loss of DO effects on DN after treatment of inhibitors of TLRs.

Keywords: Cytokines, Diabetic Nephropathies, Insulin Resistance, Toll-Like Receptors



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